4.5 Article

Untargeted LC-MS metabolomics approach reveals metabolic changes in genetically improved farmed tilapia (Oreochromis niloticus) with fatty liver induced by a high-fat diet

期刊

AQUACULTURE RESEARCH
卷 52, 期 2, 页码 724-735

出版社

WILEY
DOI: 10.1111/are.14929

关键词

fatty liver; GIFT; high-fat diet; metabolic change; metabolomic analysis

资金

  1. Special Fund of the National Natural Science Foundation of China [32002363, 31502143]
  2. Edanz Group China

向作者/读者索取更多资源

Fatty liver commonly occurs in intensively farmed tilapia, leading to impairments in hepatic lipid metabolism and disruptions to protein and carbohydrate metabolism. In this study, high-fat diet fed tilapia accumulated more fat in the liver compared to normal-fat diet fed tilapia, with differential accumulation of 36 metabolites between the two groups. These metabolic disorders may be related to the lower growth rate observed in high-fat diet fed tilapia.
Hepatic steatosis commonly occurs in intensively farmed tilapia. This disease is harmful to fish growth and health, but knowledge of the metabolic changes in tilapia with fatty liver is limited. In the present study, we compared male genetically improved farmed tilapia (GIFT,Oreochromis niloticus) fed a high-fat diet (HFD) with those fed a normal-fat diet (NFD) for 8 weeks using LC-MS-based hepatic metabolomic assays and traditional nutritional assessments. Juvenile GIFT fed a HFD accumulated more fat in the liver than did those fed a NFD. The metabolomic analyses revealed 36 differentially accumulated metabolites between the two groups, and these metabolites were involved in 25 signalling pathways. Our results indicate that development of fatty liver severely impairs hepatic lipid metabolism, leading to blockage of the TCA cycle and further disruptions to protein and carbohydrate metabolism in GIFT. These physiological changes may be related to the lower growth rate of GIFT fed a HFD. Overall, our results reveal the details of metabolic disorders in GIFT fed a HFD and enhance our knowledge of the mechanism of fatty liver formation in GIFT.

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